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- W2013039981 abstract "Data currently available on HIV-1-induced cytopathology is unclear regarding the mechanism of cell killing.To clarify the extent to which apoptosis or necrosis is involved in HIV-1-induced cell death in view of conflicting existing data.T lymphoblastoid cells or peripheral blood mononuclear cells were infected by various strains of HIV-1 and the numbers of apoptotic or necrotic cells were quantified at various times after infection using video-image analysis techniques; the results were compared with the amount of fragmented DNA using a quantitative method. Measurement of mitochondrial transmembrane potential (deltapsi(m)) and intracellular calcium concentrations [Ca2+]i was performed with fluorescent probes and fluorescence concentration analysis (FCA).Although lymphoblastoid and monocytoid cells acutely infected by HIV-1 had increased levels of fragmented DNA, a marker of apoptotic cell death, few (<12%) had condensed chromatin and fragmented nuclei, the morphological features of apoptosis. The predominant alterations in acutely infected cells were distended endoplasmic reticulum and abnormal mitochondria; these ultrastructural changes are consistent with necrosis, although some infected cells simultaneously displayed features of both necrosis and apoptosis. Viability of cells persistently infected by HIV-1 was only minimally reduced from that of uninfected cells. This reduction was accounted for by an increased propensity of the persistently infected cells to die by apoptosis. Alterations in [Ca2+]i and deltapsi(m) occurred in both acutely and persistently infected cells.Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells." @default.
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- W2013039981 date "1999-10-01" @default.
- W2013039981 modified "2023-10-07" @default.
- W2013039981 title "Both necrosis and apoptosis contribute to HIV-1-induced killing of CD4 cells" @default.
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- W2013039981 doi "https://doi.org/10.1097/00002030-199910010-00004" @default.
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